Triacylglycerols are highly concentrated stores of metabolic energy. They physiologically function as (1) fuel molecules, (2) components of phospholipids and glycolipids, (3) hydrophilic modifiers of proteins, and (4) hormones and intracellular messengers. Fatty acids are stored in adipose tissue as triglycerides. Triacylglycerols can be mobilized by the hydrolytic action of lipases that are under hormonal control. Glucagon and epinephrine can stimulate triacylglycerol breakdown by activating the lipase. Insulin, in contrast, inhibits lipolysis. Fatty acids are activated to acyl CoAs, transported across the inner mitochondrial membrane by carnitine, and degraded in the mitochondrial matrix by a recurring sequence of four reactions: oxidation by FAD, hydration, oxidation by NAD+, and thiolysis by CoA. The FADH2 and NADH formed in the oxidation steps transfer their electrons to O2 by means of the respiratory chain, whereas the acetyl CoA formed in the thiolysis step normally enters the citric acid cycle by condensing with oxaloacetate. Mammals are unable to convert fatty acids into glucose, because they lack a pathway for the net production of oxaloacetate, pyruvate, or other gluconeogenic intermediates from acetyl CoA. (Stryer, Tymoczko, & Berg, 2012, p.691).

Unsaturated and odd-chain fatty acids require additional steps for degradation. Fatty acids that contain double bonds or odd numbers of carbon atoms require ancillary steps to be degraded. An isomerase and a reductase are required for the oxidation of unsaturated fatty acids, whereas propionyl CoA derived from chains with odd numbers of carbon atoms requires a vitamin B12-dependent enzyme to be converted into succinyl CoA. (Stryer et al., 2012, p.692).

Fatty acids are synthesized in the cytoplasm by a different pathway from that of β-oxidation. Synthesis starts with the carboxylation of acetyl CoA to malonyl CoA, the committed step. This ATP-driven reaction is catalyzed by acetyl CoA carboxylase, a biotin enzyme. The intermediates in fatty acid synthesis are linked to an acyl carrier protein. Acetyl ACP is formed from acetyl CoA, and malonyl ACP is formed from malonyl CoA. Acetyl ACP and malonyl ACP condense to form acetoacetyl ACP, a reaction driven by the release of CO2 from the activated malonyl unit. A reduction, a dehydration, and a second reduction follow. NADPH is the reductant in these steps. The butyryl ACP formed in this way is ready for a second round of elongation, starting with the addition of a two-carbon unit from malonyl ACP. Seven rounds of elongation yield palmitoyl ACP, which is hydrolyzed to palmitate. In higher organisms, the enzymes catalyzing fatty acid synthesis are covalently linked in a multifunctional enzyme complex. A reaction cycle based on the formation and cleavage of citrate carries acetyl groups from mitochondria to the cytosol. NADPH needed for synthesis is generated in the transfer of reducing equivalents from mitochondria by the malate-pyruvate shuttle and by the pentose phosphate pathway. (Stryer et al., 2012 p.692).

Fatty acid synthesis and degradation are reciprocally regulated so that both are not simultaneously active. Acetyl CoA carboxylase, the essential control site, is stimulated by insulin and inhibited by glucagon and epinephrine. These hormonal effects are mediated by changes in the amounts of the active dephosphorylated and inactive phosphorylated forms of the carboxylase. Citrate, which signals an abundance of building blocks and energy, allosterically stimulates the carboxylase. Glucagon and epinephrine stimulate triacylglycerol breakdown by activating the lipase. Insulin, in contrast, inhibits lipolysis. In times of plenty, fatty acyl CoAs do not enter the mitochondrial matrix because malonyl CoA inhibits carnitine acyltransferase I. (Stryer et al., 2012, pp.692-693).

The elongation and unsaturation of fatty acids are accomplished by accessory enzyme systems. Fatty acids are elongated and desaturated by enzyme systems in the endoplasmic reticulum membrane. Desaturation requires NADH and O2 and is carried out by a complex consisting of a flavoprotein, a cytochrome, and a nonheme iron protein. Mammals lack the enzymes to introduce double bonds distal to C-9, and so they require linoleate and linolenate in their diets. Arachidonate, an essential precursor of prostaglandins and other signal molecules, is derived from linoleate. This 20:4 polyunsaturated fatty acid is the precursor of several classes of signal molecules—prostaglandins, prostacyclins, thromboxanes, and leukotrienes—that act as messengers and local hormones because of their transience. They are called eicosanoids because they contain 20 carbon atoms. Aspirin (acetysalicylate), an anti-inflammatory and antithrombotic drug, irreversibly blocks the synthesis of these eicosanoids (Stryer et al., 2012, p.692). The above is only partial explanation of the basic principles of triglyceride metabolism.

Elevated levels of triglycerides are associated with atherosclerosis, and if coupled with hypertension, would increase the risk of coronary heart disease and stroke. In addition, high levels of triglycerides will also contribute to more viscous (thicker) blood and lead to pancreatitis, which may in turn affect the function of blood in carrying oxygen, especially in the brain. Treatments for higher triglyceride levels can be divided into dietary modification and drug therapy. In the diet, we should limit the intake of carbohydrates, fat, and alcohol to maintain an ideal body weight and life style. Medications with fibric acid derivatives, bile acid sequestrates, and nicotinic acid may be prescribed for 3 to 6 months in combination with regular examination on the blood lipid concentration. Some cases even cannot be cured in the whole life.

Table 1. The triglyceride index recommended by the American Heart Association
Index(mg/dL)
 Index(µmol/L)
Remarks
 <150
 <1.69
Normal range – low risk
 150-199
 1.70-2.25
 Slightly above normal
 200-498
 2.25-5.63
Some risk
 >500
 >5.65
 Very high – high risk
Note: This table is adapted and translated from https://zh.wikipedia.org/wiki/%E4%B8%89%E9%85%B8%E7%94%98%E6%B2%B9%E9%85%AF

 

The New Human Line is a free biological system in Eukaryotic Constant Domain. The processes of biochemical reactions in the body are activated by the Absolutely Constant Energy Source (ACES). ACES can be used to regulate the free energy in the body to activate the chemical reactions of carbohydrates, lipids, proteins, amino acids, enzymes, nucleic acids, vitamins, hormones and trace elements. It will convert irreversible spontaneous processes to reversible spontaneous processes and thus deal with elevated triglyceride levels in the blood in a different way from that operating in modern human bodies.

There are 3 approaches for the New Human Line to manage with the elevated triglyceride levels in the blood, as described below:

  1. By performing strong promotion in genes: Strong promotion is applied to the DNA fragments (LYF of TG) that can rapidly lower triglycerides. These DNA fragments are located in the pancreas, liver, and the cells in the control loop regulating bile release. The triglycerides produced from the dietary intake of carbohydrates, fats, etc., can be rapidly excreted out of the body. This physiological process will proceed in about 30 minutes after meals following strong promotion in genes.
  2. By performing random promotion in genes: It can randomly metabolize excess triglycerides inside the body and expel foods which will produce triglycerides out of the body.
  3. By performing energy-mass conversion to increase the concentration of the medicine prescribed for lowering triglycerides so as to reduce triglyceride levels.

 

Figure 1. Liver, gallbladder, pancreas and bile passage.
Note: adapted from http://www.vasileiosdrakopoulos.com/en/surgical-methods/advanced-laparoscopic/laparoscopic-hepatobiliary-surgery/choledocholithiasis/

 

The following clinical trial was done by the first successfully-evolved New Human Line, Mr. Yuan Lin, who utilized the third approach of mass and energy conversion to increase the concentration of the medicine prescribed for lowering triglycerides so as to rapidly reduce triglyceride levels.

The experiment started with Mr. Yuan Lin, the first successfully-evolved New Human Line, increasing the level of triglycerides in the blood up to 700 mg/dL. He then raised up the concentration of Lipitor through the Absolutely Constant Energy Source and the new biological engineering techniques to rapidly lower triglycerides.


Figure 1. The result of the medical examination which showed that Mr. Yuan Lin increased the triglycerides in the blood up to 700 mg/dL.

 

Figure 2. The result of the medical examination taken on the 33rd day after Mr. Yuan Lin utilized the Absolutely Constant Energy Source and the new biological engineering techniques to raise the concentration of Lipitor to rapidly lower the triglycerides. It showed a nearly normal level of the triglycerides in the blood.

 


 Figure 3. The result of the medical examination taken on the 49th day, which showed that both the levels of Mr. Yuan Lin’s cholesterol and triglycerides were within the normal values.

 

From the above medical examination results, we can see that Mr. Yuan Lin, the New Human Line, can utilize the Absolutely Constant Energy Source and the new biological engineering techniques to raise the concentration of Lipitor to rapidly lower triglycerides in the body (p=0.000). It proves that Mr. Yuan Lin, the New Human Line, has the capacity to regulate triglycerides with energy.

 

References:

  1. 三酸甘油酯 (2016)。Retrieved from https://zh.wikipedia.org/wiki/%E4%B8%89%E9%85%B8%E7%94%98%E6%B2%B9%E9%85%AF
  2. Haisam Shah, BSc. (2016). High blood levels of fats are a risk factor for acute pancreatitis. Retrieved from http://www.medicalnewsbulletin.com/high-blood-levels-fats-risk-factor-acute-pancreatitis/
  3. Hypertriglyceridemia. (2016). Retrieved from https://en.wikipedia.org/wiki/Hypertriglyceridemia
  4. Stryer, L., Tymoczko, J.L., & Berg, J.M. (2012). Biochemistry. (7th ed.). New York, NY: W.H. Freeman and company.
 
 
1.
The official version of this website is written in Traditional Chinese (Taiwan).
2.
In the announcement of the research reports of the New Human Line, this website only presents the summary, experiment results and statistical analysis. The official research reports include experiment methods, results, statistical analysis and related academic theses.
3.
Mr. Yuan Lin is the only authentic New Human Line that has passed the verification of the Bodhi humans.
4.
All the related knowledge of the New Human Line is protected by Intellectual Property Rights and Trade Secret Act.
   

This website for the Association for the Human Evolution (the “Association”) is used for the purpose of presenting research papers only. The Association makes no warranties of any kind, express or implied about the completeness with respect to the website or the information on the website for any purpose. No offer or attempt to lobby is made by the Association for the use of the material or information on this website as a basis for any purpose. All the new physiological functions mentioned in the contents of this website are the specific mechanisms unique to the New Human Line and may undergo alteration, evolution and change as the environment changes. The Association hereby assumes no responsibility for automatically updating the contents of this website in case of any related change hereafter.

Anyone that browses, learns from, or even imitates the contents of this website shall carefully consider all sorts of information and prudently evaluate his or her own physical status. You assume all responsibility for and risk arising from the use of and reliance upon the contents of this website. To the extent not prohibited by law, in no circumstances shall the Association and its members and the presenter of the research paper be liable to you or any other third parties for any loss or damage arising directly or indirectly, specifically, accidentally or causatively from the use of or your acts based on the contents of this website or any of the material contained in it.

 
 
 
  U.S.A.:
  95 Linhaven,
  Irvine, CA. 92602  
  U.S.A.
 
Taiwan:
2F., No.76, Zhongxin St.,
Xinzhuang Dist., New Taipei City 242,
Taiwan (R.O.C.)
 
Research Center:
No.7-7, Shunxing Rd.,
Shuilin Township, Yunlin County 652, Taiwan (R.O.C.)
 
Carbon-oxygen Laboratory:
No.7-1, Shunxing Rd.,
Shuilin Township, Yunlin County 652, Taiwan (R.O.C.)
 
The copyright belongs to Mr. Yuan Lin and he reserves all legal right.